| |
| The summaries are free for public
use. The Chronic Liver Disease
Foundation will continue to add and
archive summaries of articles deemed
relevant to CLDF by the Board of
Trustees and its Advisors. |
| |
|
|
| Abstract Details |
 |
|
| |
| |
| |
|
|
| |
Brain magnetic resonance spectroscopy in episodic hepatic encephalopathy |
|
|
|
|
| |
Chavarria L, Alonso J, García-Martínez R, Simón-Talero M, Ventura-Cots M, Ramírez C, Torrens M, Vargas V, Rovira A, Córdoba J. J Cereb Blood Flow Metab. 2012 Nov 21. doi: 10.1038/jcbfm.2012.173. [Epub ahead of print] |
|
| |
|
|
| |
Source
1] Liver Unit, Hospital Vall d'Hebron, Barcelona, Spain [2] Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain [3] Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain.
Abstract
Brain magnetic resonance (MR) study has shown metabolic abnormalities and changes in water distribution of the brain tissue that may relate to the pathogenesis of hepatic encephalopathy (HE). We designed a study to investigate the disturbances in brain water and metabolites during episodic HE using a 3-T MR scanner. Cirrhotic patients with different grades of HE underwent MR during hospitalization (n=18). The MR was repeated at 6 weeks' follow-up (n=14). The results were compared with those of a group of healthy volunteers (n=8). During episodic HE, brain diffusion-weighted imaging showed a high apparent diffusion coefficient (ADC) (12% to 14%) that decreased during follow-up (-1% to -4%). These disturbances were accompanied by high glutamine (581%), low choline (-31%), and low myo-inositol (-86%) peaks on MR spectroscopy. In overt HE, patients showed high glutamine that decreased during follow-up (-22%). In addition, these patients exhibited a rise in plasma S100 beta and enlargement of brain white-matter lesions. In conclusion, several disturbances detected by MR support the presence of impaired brain water homeostasis during episodic HE. Although astrocytes have a major role in this condition, brain edema during episodic HE may be extracellular and does not appear to be directly responsible for the development of neurologic manifestations.
|
|
|
|
| |
| |
|